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Method of treating age-related macular degeneration

a macular degeneration and age-related technology, applied in the field of age-related macular degeneration treatment, can solve the problems of visual impairment, over-activation of the immune system, and contributing to disease pathogenesis

Pending Publication Date: 2022-08-18
THE PROVOST FELLOWS FOUND SCHOLARS & THE O
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  • Summary
  • Abstract
  • Description
  • Claims
  • Application Information

AI Technical Summary

Benefits of technology

The patent describes a method that can protect the photoreceptor cells in the retina from dying or being damaged. This can be done by reducing the amount of oxidative stress that can occur in the retina. The method can also prevent the retinal pigment epithelium, which is a layer of cells that supports the photoreceptor cells, from breaking down and causing damage. Overall, this method can help to maintain the health of the retina and improve vision.

Problems solved by technology

Excessive oxidative stress induces deleterious changes that result in visual impairment.
As these stimuli are often not easily cleared, they can persist causing over-activation of the immune system and contributing to disease pathogenesis.

Method used

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  • Method of treating age-related macular degeneration
  • Method of treating age-related macular degeneration
  • Method of treating age-related macular degeneration

Examples

Experimental program
Comparison scheme
Effect test

example 2

[0090]AMD-Associated Oxidative Stress Products Induce AP Complement Secretion from hfRPE Cells

[0091]It was next assessed whether a physiologically relevant DAMP generated by oxidative stress could induce the same response in primary human fetal RPE (hfRPE) cells. The retina is one of the most highly metabolically active tissues in the body. This oxidative burden, results in generation of lipid oxidation products such as CEP (FIG. 11). hfRPE cells were incubated with either a neutralizing antibody targeting TLR2 (anti-TLR2) or an IgG control prior to stimulation with CEP-adducted to human serum albumin (CEP-HSA). CEP-HSA induced C3 and CFB transcripts to similar levels observed for Pam3Cys4 in RPE cells and this was inhibited by the presence of anti-TLR2 neutralizing antibodies (FIG. 1m, n). TLR2 localization was assayed in human donor eye tissue and observed both apically and basolaterally in the plasma membrane of the RPE (FIG. 10) Immunoblot analysis demonstrated TLR2 effect on tr...

example 3

Neutralization of TLR2 in a Photo-Oxidative Stress Model of Retinal Degeneration Decreases C3 Deposition and Promotes Survival of Photoreceptor Cells

[0092]Overexpressing C3 in the retina can promote many features of AMD, while inhibiting various complement factors can protect against photoreceptor cell death in models of retinal degeneration. To define a role for TLR2 in bridging oxidative stress to complement activation and assessing its function in retinal degeneration, a well-characterized light-induced photo-oxidative stress model of retinal degeneration was utilized, in which locally produced C3 is known to contribute causally to retinal degeneration. In this model, there is a significant increase in C3+ macrophage / microglia in the photoreceptor layer and a decrease in outer nuclear layer (ONL) thickness. The ONL is made up of the nuclei of the rod and cone photoreceptors, and a decrease in the ONL thickness is indicative of photoreceptor cell death and retinal degeneration. An...

example 4

Inhibiting Amplification of the AP Ameliorates RPE Degeneration in the NaIO3 Model of Retinal Degeneration

[0093]The NaIO3 mouse model of oxidative stress mimics some features of human retinal disease albeit in an acute manner; notably complement deposition, RPE fragmentation and photoreceptor cell degeneration. In vitro, NaIO3 dose dependently induced the expression of TLR2, CFB and C3 in RPE cells (FIG. 10), indicating the potential for activation of both TLR2 pathways and the AP in this model. Although there are potentially many DAMPs that drive TLR activation in response to oxidative damage, the appearance of CEP adducts was tested. FIG. 11 clearly demonstrates presence of CEP lipid oxidation product in the photoreceptor layer (3rd column) in NaIO3 treated animals, when compared to saline and IgG-control sections (1st and 2nd columns). CEP appears strongly in the central retina, with weaker staining in peripheral retina, a phenomena also observed in a high glycemic diet-induced m...

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Abstract

The present invention relates to a method of treating age-related macular degeneration. In particular embodiments, the invention relates to methods of treating age-related macular degeneration in a subject in need thereof, the method comprising the step of decreasing the expression or activation of a toll-like receptor in the subject.

Description

CROSS-REFERENCE TO RELATED APPLICATIONS[0001]This application claims benefit of priority of U.S. Provisional Patent Application No. 63 / 150,177 entitled, “A METHOD OF TREATING AGE-RELATED MACULAR DEGENERATION”, filed Feb. 17, 2021. The entire contents and disclosures of these patent applications are incorporated herein by reference in their entirety.FIELD OF THE INVENTION[0002]The present invention relates to a method of treating age-related macular degeneration. In particular embodiments, the invention relates to methods for treating dry age-related macular degeneration.BACKGROUND TO THE INVENTION[0003]Age-related macular degeneration (AMD) is the leading cause of central blindness in adults. Dry AMD (also called nonexudative AMD) is a broad designation, encompassing forms of AMD that are not neovascular. At present, there are no treatments for dry AMD. Genetic factors, age, diet and smoking are risk factors for AMD.[0004]The common, coding variant Y402H in the Complement Factor H (...

Claims

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Application Information

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Patent Type & Authority Applications(United States)
IPC IPC(8): A61K31/713A61K38/00C12N15/115C12N15/113A61P27/02
CPCA61K31/713A61K38/00A61P27/02C12N15/1138C12N15/115
Inventor DOYLE, SARAHCAMPBELL, MATTHEWOZAKI, EMAMULFAUL, KELLY
Owner THE PROVOST FELLOWS FOUND SCHOLARS & THE O
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